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Helicobacter pylori induces IL-1β protein through the inflammasome activation in differentiated macrophagic cells
Title: | Helicobacter pylori induces IL-1β protein through the inflammasome activation in differentiated macrophagic cells |
Authors: | Kameoka, Shoichiro Browse this author | Kameyama, Takeshi Browse this author →KAKEN DB | Hayashi, Takaya Browse this author | Sato, Seiichi Browse this author | Ohnishi, Naomi Browse this author | Hayashi, Takeru Browse this author | Murata-Kamiya, Naoko Browse this author | Higashi, Hideaki Browse this author →KAKEN DB | Hatakeyama, Masanori Browse this author →KAKEN DB | Takaoka, Akinori Browse this author →KAKEN DB |
Issue Date: | Feb-2016 |
Publisher: | Biomedical Research Press |
Journal Title: | Biomedical Research |
Volume: | 37 |
Issue: | 1 |
Start Page: | 21 |
End Page: | 27 |
Publisher DOI: | 10.2220/biomedres.37.21 |
PMID: | 26912137 |
Abstract: | More than 50% of people in the world are infected with Helicobacter pylori (H. pylori), which induces various gastric diseases. Especially, epidemiological studies have shown that H. pylori infection is a major risk factor for gastric cancer. It has been reported that the levels of interleukin (IL)-1β are upregulated in gastric tissues of patients with H. pylori infection. In this study, we investigated the induction mechanism of IL-1β during H. pylori infection. We found that IL-1βmRNA and protein were induced in phorbol-12-myristate-13-acetate (PMA)-differentiated THP-1 cells after H. pylori infection. This IL-1β production was inhibited by a caspase-1 inhibitor and a ROS inhibitor. Furthermore, K+ efflux and Ca2+ signaling were also involved in this process. These data suggest that NOD-like receptor (NLR) family, pyrin domain containing 3 (NLRP3) and its complex, known as NLRP3 inflammasome, are involved in IL-1β production during H. pylori infection because it is reported that NLRP3 inflammasome is activated by ROS, K+ efflux and/or Ca2+ signaling. These findings may provide therapeutic strategy for the control of gastric cancer in H. pylori-infected patients. |
Type: | article |
URI: | http://hdl.handle.net/2115/61351 |
Appears in Collections: | 遺伝子病制御研究所 (Institute for Genetic Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)
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Submitter: 高岡 晃教
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